RESUMO
ABSTRACT Objective: To investigate the effectiveness of Suresmile® lingual therapy on torque, tip, and rotations measures through digital evaluation of planning and post-treatment digital models. Material and Methods: A sample of 12 Caucasian adult patients (4 men; mean age 30.6 years ± 3.9 and 8 women; mean age 31.4 years ± 4.5) treated with the Suresmile® lingual orthodontic technique was retrospectively selected, regardless of the type of malocclusion. Digital planning was performed with Suresmile® software, while lingual therapy was accomplished with interactive self-ligating lingual brackets and customized Suresmile® arches. First, digital models of planning and post-treatment digital models were compared using VAM software (and the discrepancies were analyzed through MANOVA and four multivariate. Then, Tukey and Bonferroni's post-hoc tests are performed. Results: The accuracy average values are 60.11 ± 27.67% for torque, 53.52 ± 27.37% for tip and 59.19 ± 26.42% for rotation, while for inaccuracy values are 2.72° ± 2.23° for torque, 2.98° ± 2.16°for tip and 3.58° ± 3.29° for rotation. No significant differences have been recorded evaluating different sectors of both arches. Conclusion: This retrospective preliminary study highlight how overcorrections, especially in the Suresmile lingual technique, should be performed during orthodontic planning. Moreover, the study gets bases for further, more structured future studies that should involve larger and more homogeneous samples.
Assuntos
Humanos , Feminino , Adulto , Braquetes Ortodônticos , Oclusão Dentária , Estética Dentária , Aparelhos Ortodônticos Fixos , Má Oclusão , Projetos Piloto , Análise Multivariada , Estudos Retrospectivos , Estatísticas não Paramétricas , ItáliaRESUMO
BACKGROUND: HER2-overexpression promotes malignancy by modulating signalling molecules, which include PTPs/DSPs (protein tyrosine and dual-specificity phosphatases). Our aim was to identify PTPs/DSPs displaying HER2-associated expression alterations. METHODS: HER2 activity was modulated in MDA-MB-453 cells and PTPs/DSPs expression was analysed with a DNA oligoarray, by RT-PCR and immunoblotting. Two public breast tumor datasets were analysed to identify PTPs/DSPs differentially expressed in HER2-positive tumors. RESULTS: In cells (1) HER2-inhibition up-regulated 4 PTPs (PTPRA, PTPRK, PTPN11, PTPN18) and 11 DSPs (7 MKPs [MAP Kinase Phosphatases], 2 PTP4, 2 MTMRs [Myotubularin related phosphatases]) and down-regulated 7 DSPs (2 MKPs, 2 MTMRs, CDKN3, PTEN, CDC25C); (2) HER2-activation with EGF affected 10 DSPs (5 MKPs, 2 MTMRs, PTP4A1, CDKN3, CDC25B) and PTPN13; 8 DSPs were found in both groups. Furthermore, 7 PTPs/DSPs displayed also altered protein level. Analysis of 2 breast cancer datasets identified 6 differentially expressed DSPs: DUSP6, strongly up-regulated in both datasets; DUSP10 and CDC25B, up-regulated; PTP4A2, CDC14A and MTMR11 down-regulated in one dataset. CONCLUSIONS: Several DSPs, mainly MKPs and, unexpectedly, MTMRs, were altered following HER2-modulation in cells and 3 DSPs (DUSP6, CDC25B and MTMR11) were altered in both cells and tumors. Among these, DUSP6, strongly up-regulated in HER2-positive tumors, would deserve further investigation as tumor marker or potential therapy target.